Therapeutic potential of Bifidobacterium breve strain A1 for preventing cognitive impairment in Alzheimer’s disease

Abstract

It has previously been shown that the consumption of probiotics may have beneficial effects not only on peripheral tissues but also on the central nervous system and behavior via the microbiota–gut–brain axis, raising the possibility that treatment with probiotics could be an effective therapeutic strategy for managing neurodegenerative disorders. In this study, we investigated the effects of oral administration of Bifidobacterium breve strain A1 (B. breve A1) on behavior and physiological processes in Alzheimer’s disease (AD) model mice. We found that administration of B. breve A1 to AD mice reversed the impairment of alternation behavior in a Y maze test and the reduced latency time in a passive avoidance test, indicating that it prevented cognitive dysfunction. We also demonstrated that non-viable components of the bacterium or its metabolite acetate partially ameliorated the cognitive decline observed in AD mice. Gene profiling analysis revealed that the consumption of B. breve A1 suppressed the hippocampal expressions of inflammation and immune-reactive genes that are induced by amyloid-β. Together, these findings suggest that B. breve A1 has therapeutic potential for preventing cognitive impairment in AD.

The role of gut microbiota in pathogenesis of Alzheimer's disease

“…) , which can augment inflammation level in the plasma and subsequently in CNS (Kobayashi et al . ). These data present a hypothesis that gut microbiomes have strong connections with the pathogenesis of AD and diminished microbiota diversity can trigger several pathologies in the brain such as inflammation, cerebrovascular degeneration, Aβ aggregation and tau pathology.…”

“…In addition to this in vitro study, Kobayashi et al . () investigated the effect of acetate on behavioural and working memory deficits in an AD model induced by intracerebral Aβ 25‐35 injection and observed that behavioural deficits in the mice were ameliorated. Interestingly, the improvement in behavioural deficits with the administration of acetate was also observed upon orally administrating sonicated B. breve strain A1 ( B. breve A1) homogenate.…”

“…These dose-dependent effects of gut metabolites show that reduction in the amount of beneficial metabolite secreted by the anti-inflammatory bacteria in the intestinal flora may promote Ab accumulation in the brain. In addition to this in vitro study, Kobayashi et al (2017) investigated the effect of acetate on behavioural and working memory deficits in an AD model induced by intracerebral Ab [25][26][27][28][29][30][31][32][33][34][35] injection and observed that behavioural deficits in the mice were ameliorated. Interestingly, the improvement in behavioural deficits with the administration of acetate was also observed upon orally administrating sonicated B. breve strain A1 (B. breve A1) homogenate.…”

“…In summary, the most distinctive alterations in gut microbiome flora observed in AD are decreasing of the abundance of anti-inflammatory bacterial species such as Bifidobacterium breve strain A1 and increasing the abundance of pro-inflammatory bacterial species such as Firmicutes and Bacteroidetes (Fig. 2), which can augment inflammation level in the plasma and subsequently in CNS (Kobayashi et al 2017). These data present a hypothesis that gut microbiomes have strong connections with the pathogenesis of AD and diminished microbiota diversity can trigger several pathologies in the brain such as inflammation, cerebrovascular degeneration, Ab aggregation and tau pathology.…”

Therapeutic Microbiology: the Role of <em>Bifidobacterium Breve</em> as Food Supplement for the Prevention/Treatment of Pediatric Diseases

“…Savignac et al [88] showed that 6 weeks feeding of B. breve 1205 strain resulted in positive effects on compulsive behaviour in marble burying test, anxiolytic effects in the elevated plus maze and reduced bodyweight gain in model mice, contributing to a general amelioration of anxiety and metabolism. Kobayashi et al [89] showed that oral administration of B. breve A1, isolated from feces of human infants, prevented cognitive decline in Alzheimer disease (AD) model mice, with a reduction of neural inflammation; they observed that the probiotic provided ameliorations in both working memory and long-term memory. Furthermore, they found an increase of plasma acetate levels after the probiotic treatment and the neural inflammation reduction can be considered as a consequence of this increase due to B. breve administration, since SCFAs have been shown to have immune modulatory functions in model mice [90].…”